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Nasal Vaccine Might Slow Alzheimer's

Mouse study showed 73 percent reduction in damaging amyloid plaques

THURSDAY, Aug. 11, 2005 (HealthDay News) -- Researchers think they are close to devising a deceptively simple way to prevent the progression of Alzheimer's disease: a nasal spray vaccine.

Although it has so far only been tested on mice, the vaccine is a combination of two medications -- Protollin and glatiramer acetate, which has already been approved to treat other conditions, such as multiple sclerosis (MS).

The spray targets what many researchers suggest is the most probable cause of Alzheimer's -- the abnormal build-up in the brain of a sticky substance called beta-amyloid plaque.

"This is a vaccine in the scientific sense of the word, in that I'm very hopeful it could stimulate the immune system to reduce this build-up among people with early signs of Alzheimer's as well as for those in later stages of the disease," said study co-author Dr. Howard L. Weiner, co-director of the Center for Neurologic Diseases at Brigham and Women's Hospital in Boston.

Weiner and his colleagues detail their work in the Aug. 11 online issue of the Journal of Clinical Investigation.

To date, scientific proof has not quite reached the critical mass whereby amyloid accumulation is acknowledged as the main source of the memory and cognition problems that are the paramount manifestations of Alzheimer's.

Nonetheless, the notion is the subject of many ongoing studies, and it increasingly dominates efforts to improve treatments for a disease that strikes more than 18 million across the globe. That figure is expected to grow dramatically as life expectancy rises; the disease already lays claim to being the most common form of senile dementia.

With vaccine research, scientists have at times run into unforeseen problems. In one trial, animal work with a traditional vaccine design that sought to provoke the development of antibodies to eliminate amyloid led to the development of encephalitis -- a dangerous inflammation of the brain.

Weiner and his colleagues took a different approach, designing a vaccine -- administered via drops in the nose -- that would initiate an amyloid-cleansing process by triggering the immune system without provoking antibody development.

The researchers targeted a specific type of amyloid-eating cell known as a microglial cell -- stimulating the cells into action to essentially gobble up the amyloid build-up.

Before the study, the mice had been determined to have a build-up of beta-amyloid plaque in their brains in amounts similar to what would be present in a human Alzheimer's patient.

The vaccine was administered to the mice on a weekly basis for six weeks, after an initial grouping of four doses was given within the first week.

The research team began monitoring the mice one week after vaccination began, looking for signs of disease, paralysis, limb weakness and fatigue. Ultimately, brain tissue was dissected and examined for evidence of both amyloid quantity and any toxic side effects that might have developed in reaction to the vaccine.

The authors found that, overall, amyloid plaque levels in the vaccinated mice were reduced by 73 percent. None of the vaccinated mice showed any evidence of encephalitis or other toxic side effects.

Weiner and his team said they hope to begin small-scale testing of the Alzheimer's nasal spray vaccine in people by 2006, following talks this fall with the U.S. Food and Drug Administration. They noted that the human trial process will play out over a number of years, so a nasal Alzheimer's vaccine is -- at best -- several years away from clinical use.

Weiner noted that although there are a number of different research projects currently exploring the potential of amyloid reduction, none has yet been shown to work in people. And he emphasized that transitioning from animals to people is a tricky process that doesn't always work.

"But I'm very enthusiastic," he said. "I think it has a good chance of working and helping Alzheimer's patients -- and even opening up a new avenue for developing a vaccine for MS."

Dr. Sam Gandy, vice president of the medical and scientific advisory council of the Alzheimer's Association, shared a similar sense of hope.

"I think this is very interesting," said Gandy. "It's really sort of unexpected, because most everyone in the field has based their approaches on some compound that was specifically related to amyloid and amyloid antibodies. And this work shows that you can perhaps do this in a non-antibody way -- avoiding encephalitis, which is an important plus. It will be exciting to see this develop."

More information

For more on Alzheimer's, check the Alzheimer's Association.

SOURCES: Howard L. Weiner, M.D., co-director, Center for Neurologic Diseases, Brigham and Women's Hospital, Boston; Sam Gandy, M.D., vice president, medical and scientific advisory council. Alzheimer's Association, Chicago; Aug. 11, 2005, Journal of Clinical Investigation online
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